The DOI matches its Crossref record; 31 of the 31 references it cites were found in a registry or an index.
Fus deficiency in mice results in defective B-lymphocyte development and activation, high levels of chromosomal instability and perinatal death
Abstract
The gene FUS (also known as TLS (for translocated in liposarcoma) and hnRNP P2) is translocated with the gene encoding the transcription factor ERG-1 in human myeloid leukaemias. Although the functions of wild-type FUS are unknown, the protein contains an RNA-recognition motif and is a component of nuclear riboprotein complexes. FUS resembles a transcription factor in that it binds DNA, contributes a transcriptional activation domain to the FUS-ERG oncoprotein and interacts with several transcription factors in vitro. To better understand FUS function in vivo, we examined the consequences of disrupting Fus in mice. Our results indicate that Fus is essential for viability of neonatal animals, influences lymphocyte development in a non-cell-intrinsic manner, has an intrinsic role in the proliferative responses of B cells to specific mitogenic stimuli and is required for the maintenance of genomic stability. The involvement of a nuclear riboprotein in these processes in vivo indicates that Fus is important in genome maintenance.
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“Fus-null mice die soon after birth179”
From The neurogenetics of alternative splicing (2016) · cites this paper as [179]
Citations
Cites
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Atm-Deficient Mice: A Paradigm of Ataxia Telangiectasia
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Interaction between ATM protein and c-Abl in response to DNA damage
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Dual roles of ATM in the cellular response to radiation and in cell growth control.Preprint
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Self-citationTransitional B cells are the target of negative selection in the B cell compartment.
Carsetti, R., Köhler, G., & Lamers, M. C. (1995) · The Journal of Experimental Medicine · doi:10.1084/jem.181.6.2129 · Cited by 358
A human RNA polymerase II complex associated with SRB and DNA-repair proteins
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Sorted by citations
Mutations in the FUS/TLS Gene on Chromosome 16 Cause Familial Amyotrophic Lateral Sclerosis
Kwiatkowski, T. J., Bosco, D. A., LeClerc, A. L., Tamrazian, E., Vanderburg, C. R., Russ, C., Davis, A., Gilchrist, J. M., Kasarskis, E. J., Munsat, T. L., et al. (2009) · Science · doi:10.1126/science.1166066 · Cited by 2,624
Converging Mechanisms in ALS and FTD: Disrupted RNA and Protein Homeostasis
Ling, S.-C., Polymenidou, M., & Cleveland, D. W. (2013) · Neuron · doi:10.1016/j.neuron.2013.07.033 · Cited by 1,811
“Two independent FUS/TLS knockout mouse models have been generated (Kuroda et al., 2000; Hicks et al., 2000).”
TDP-43 and FUS/TLS: emerging roles in RNA processing and neurodegeneration
Lagier-Tourenne, C., Polymenidou, M., & Cleveland, D. W. (2010) · Human Molecular Genetics · doi:10.1093/hmg/ddq137 · Cited by 1,021
Induced ncRNAs allosterically modify RNA-binding proteins in cis to inhibit transcription
Wang, X., Arai, S., Song, X., Reichart, D. R., Du, K., Pascual, G., Tempst, P., Rosenfeld, M. G., Glass, C. K., & Kurokawa, R. (2008) · Nature · doi:10.1038/nature06992 · Cited by 1,007
“S5b), while the N-terminus (1-211) interacted with CBP (Fig.”
BackgroundTDP-43 and FUS in amyotrophic lateral sclerosis and frontotemporal dementia
Mackenzie, I. R., Rademakers, R., & Neumann, M. (2010) · The Lancet Neurology · doi:10.1016/s1474-4422(10)70195-2 · Cited by 1,012
Metadata
- Authors
- Hicks, G. G., Singh, N., Nashabi, A., Mai, S., Bozek, G., Klewes, L., Arapovic, D., White, E. K., Koury, M. J., Oltz, E. M., Van Kaer, L., & Ruley, H. E.
- Affiliations
- University of Manitoba (CA)
- Howard Hughes Medical Institute (US)
- Vanderbilt University (US)
- Corresponding author
- Hicks, Geoffrey G.
- Venue
- Nature Genetics
- Published
- 2000-02
- Volume
- 24
- Issue
- 2
- Pages
- 175-179
- ISSN
- 1061-4036 (ISSN-L)
- 1546-1718
- OpenAlex
- W2080964315
- Cited by
- 299
- References
- 31
- Citations by year
- 2026: 5 · 2025: 3 · 2024: 4 · 2023: 10 · 2022: 17 · 2021: 19 · 2020: 10 · 2019: 17 · 2018: 21 · 2017: 10 · 2016: 26 · 2015: 12 · 2014: 18 · 2013: 23 · 2012: 13
- FWCI
- 2.51
- Type
- journal article
- Language
- en
- Open access
- closed
- Licence
- www.springer.com/tdm (tdm)
- Locations
- Nature Genetics (publishedVersion)
- PubMed (publishedVersion)
- Funders
- National Institutes of Health (2r01hg000684-04a1)
- National Human Genome Research Institute (R01HG00684)
- National Cancer Institute (P30CA042014)
- National Center for Research Resources (R01RR013166)
- Topics
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › DNA Repair Mechanisms
- Life Sciences › Immunology and Microbiology › Immunology › T-cell and B-cell Immunology
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Genomics and Chromatin Dynamics
- Keywords
- FUS gene, TLS, B cell development, B cell activation, chromosomal instability, genome stability, perinatal lethality, nuclear ribonucleoprotein, transcription factors
- MeSH terms
- Animals, Animals, Newborn, B-Lymphocytes, Bone Marrow Cells, Chimera, Crosses, Genetic, Female, Genotype, Humans, Liver, Lymphocyte Activation, Male, Mice, Inbred C57BL, Ribonucleoproteins, Spleen, Restriction Mapping, RNA-Binding Proteins, Mice, Knockout, Heterogeneous-Nuclear Ribonucleoproteins, RNA-Binding Protein FUS, Mice
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